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also renal conditions Flashcards

1
Q

which of the following drugs do NOT cause hyperkalaemia: spirolonolactone, ramipril, amiloride, furosemide, atenolol

A

furosemide - causes HYPOkalaemiea

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2
Q

A newborn baby is noted to have large palpable masses in the loins and dysmorphic features consistent with Potter’s syndrome. Further investigations show renal impairment and liver fibrosis

A

autosomal recessive polycystic kidney disease

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3
Q

A 35-year-old man who has a history of hypertension and subarachnoid haemorrhage presents with recurrent UTIs and episodic haematuria

A

autosomal dominant polycystic kidney disease

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4
Q

AD polycystic kidney disease is cause by a gene mutation on which chromosome?

A

chromosome 4

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5
Q

defect in gene located on chromosome 6 which encodes fibrocystin

A

autosomal recessive polycystic kidney disease

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6
Q

mutation on chromosome 16 or 4 affecting renal tubule development

A

autosomal dominant polycystic kidney disease

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7
Q

inheritance pattern in Alport’s syndrome

A

X linked

disorder of type IV collagen matrix
mutation in COL4A5 - deficient collagen matrix deposition

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8
Q

presentation of Alport’s syndrome

A

haematuria (microscopic)
CKD
sensorineural hearing loss
ocular abnormalities - anterior lenticonus, change prescription lots

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9
Q

investigation findings of Alport’s syndrome

A

microscopic haematuria
RBC casts
renal biopsy = variable thickening of GBM
EM = splitting of lamina densa

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10
Q

anderson fabrys disease presentation

A

x linked

renal failure
angiokeratomas
cardiomyopathy, valvular disease
neuro stroke
psychiatric
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11
Q

investigations + management of anderson fabrys disease

A

absent/low levels of alpha-glactosidase A in leukocytes or plasma
renal biopsy

management = fabryzyme (enzyme replacement therapy)

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12
Q

what does nephritic syndrome indicate? which cells does it affect?

A

indicative of proliferative process

affecting endothelial cells

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13
Q

what does nephrotic syndrome indicate? which cells does it affect?

A

indicative of NON-proliferative process

affects podocytes

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14
Q

criteria for nephritic syndrome

A

haematuria
oliguria = reduced urine output
proteinuria <3g/24hr
fluid retention causing oedema

hypertension
active urinary sediments - RBCs, RBC casts

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15
Q

commonest cause of nephrotic syndrome in kids + adults respectively?

A

kids = minimal change diease

adults = focal segmental glomerulosclerosis

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16
Q

nephrotic syndrome criteria

A

peripheral oedema - ankle pitting
protein uria >3g = “frothy urine”
serum albumin <25
hypercholesterolaemia

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17
Q

how would damage to endothelial or mesangial cells present

A

red cells in urine + proliferative

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18
Q

how would damage to podocytes present

A

protein in urine (frothy) + non-proliferative

podocytes atrophy ->creates big gaps -> loss of specific/selective barrier

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19
Q

what does curved RBCs on urine microscopy indicate?

A

extra capillary proliferation or inflammation within bowmans space
–> curved RBCs squezzing through damaged enothelium

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20
Q

damage to mesangial cells

A

mesangial cells proliferate

  • release angiotensin II -> increase bp
  • release chemokines -> attracts inflammatory cells
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21
Q

damage to endothelium

A

rapid injury -> vasculitis
rapid influx of inflam cells
leakage of these through damaged endothelium wall

22
Q

minimal change GN

A

affects podocytes
commonest cause of nephrotic syndrome in KIDS
LM + IF normal
EM = podocye foot process dusion

mx = steroids

23
Q

commonest cause of idiopathic nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis (FSGS)

24
Q

what can Focal segmental glomerulosclerosis (FSGS) be secondary to?

A

HIV
heroin use (IVDU)
obesity

25
Q

histology of membranous nephropathy

A

IgG + complement deposits on basement membrane

“spikes” on silver stain

26
Q

anibody assoc with Membranous nephropathy

A

anti PLAS2r antibody

27
Q

Membranoproliferative glomerulonephritis on silver stain

A

“tram tracks”

28
Q

2 primary mechanisms of Membranoproliferative glomerulonephritis

A
  1. immune complex deposition + complement activation

2. dysregulation of alternative complement pathway

29
Q

classic presentation of IgA nephropathy

A

macroscopic haematuria in young people 1-2days post upper respiratory tract infection

30
Q

IgA nephropathy (Berger’s disease) assoc conditions

A

** henoch-schonlein purpura **

alcoholic cirrhosis
coelia/dermatitis herpetiformis

31
Q

IgA nephropathy (Berger’s disease) histology

A

mesangial hypercellularity, positive immunofluorescence for IgA + C3

(mesangial deposition of IgA immune complexes)

32
Q

causes of Rapidly progressive glomerulonephritis (RPGN)

A

ANCA +ve

  • granulomatosis with polyangiitis (wegners)
  • microscopic polyangiitis (MPA)

ANCA -ve

  • goodpastures (anti-GBM)
  • henoch-schlein purpura
  • SLE
33
Q

Rapidly progressive glomerulonephritis (RPGN) histology

A

glomerular crescents

34
Q

what type of hypersensitivity reaction in Goodpastures syndrome?

A

type 2

35
Q

goodpastures

A

anti-GBM (glomerular basement membrane) antivbodies attack glomerulus + pulmonary basement membranes
–> causes GN + pulmonary haemorrhage

antibodies specific to type IV collagen in basement membrane
assoc with HLAA DR2

36
Q

goodpastures on renal biopsy

A

linear IgG deposits along basement membrane

37
Q

management of goodpastures

A

plasma exchange

steroids

38
Q

differential diagnoses for acute renal failure + haemoptysis

A

goodpastures - anti-GM

granulomatosis with polyangiitis (wegners)

  • ANCA
  • wheeze, sinusitis, saddle shaped nose
39
Q

renal cell carcinoma

A

adenocarcinoma arises from renal tubules
commonest type of kiney tumour

often renal vein involvement - can extent into vena cava + grow up to heart

40
Q

types of renal cell carcinoma

A

clear cell - 80%
papillary - 15%
chromophobe - 5%

Wilms tumour = in kids, under 5

41
Q

presentation of renal cell carcinoma

A

triad = haematuria, flank pain, palpable mass

anaemia
polycythaemia = high conc of RBC
hypertension

42
Q

T staging of renal cell carcinoma

A

o 1 = <7cm + confined to kidney
o 2 = >7cm but confined to kidney
o 3 = local spread to nearby tissues or veins, but not beyond gerota’s fascia
IVC, renal vein
o 4 = spread beyond Gerota’s fascia, including metastasis

42
Q

T staging of renal cell carcinoma

A 
1 = <7cm + confined to kidney
2 = >7cm but confined to kidney

3 = local spread to nearby tissues or veins, but not beyond gerota’s fascia
–> IVC, renal vein
4 = spread beyond Gerota’s fascia, including metastasis

43
Q

management

A

small (<3-4cm) - observe, ablation in young
medium - ablation, partial nephrectomy
large - radical nephrectomy

surgery preffered in young, ablation back up

44
Q

clear cell carcinoma

A

loss of von hippel landau (VHL) gene on short chromosome 3

bright yellow tumour
cannonball metastases in lung

45
Q

risk factors for clear cell carcinoma

A

obesity

von hippel-lindau disease

46
Q

chromophobe (renal cell carcinoma) histology

A

v similar to oncocytome (benign), very pink granular cytoplasm

oncocytic but with raisonoif nuclei + perinuclear haloes

47
Q

oncocytoma presentation

A

mahogany brown with central stella star

incidental (85%), loin pain, haematuria

48
Q

angiomyolipoma

A

blood vessels, immature smooth muscle + fat

80% sporadic in middle aged women
20% assoc with tuberous sclerosis (auto dom)

49
Q

dibetic nephropathy presentation

A

BM thickening
Kimmelstiel-Wilson nodules

proteinuria
recurrent infections - pyelonephritis

renal (15 decks)

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